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学科主题基础医学
High-throughput cell-based screening reveals a role for ZNF131 as a repressor of ERalpha signaling
Han, Xiao2; Guo, Jinhai2; Deng, Weiwei2; Zhang, Chenying2; Du, Peige1; Shi, Taiping2,3,4; Ma, Dalong2,3,4
刊名BMC GENOMICS
2008-10-11
DOI10.1186/1471-2164-9-476
9期:0
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biotechnology & Applied Microbiology ; Genetics & Heredity
研究领域[WOS]Biotechnology & Applied Microbiology ; Genetics & Heredity
关键词[WOS]ESTROGEN-RECEPTOR-ALPHA ; HUMAN BREAST-CANCER ; MCF-7 CELLS ; TRANSCRIPTIONAL ACTIVITY ; EXPRESSION ; GENES ; PS2 ; PROLIFERATION ; CDNA ; BETA
英文摘要

Background: Estrogen receptor alpha (ER alpha) is a transcription factor whose activity is affected by multiple regulatory cofactors. In an effort to identify the human genes involved in the regulation of ER alpha, we constructed a high-throughput, cell-based, functional screening platform by linking a response element (ERE) with a reporter gene. This allowed the cellular activity of ER alpha, in cells cotransfected with the candidate gene, to be quantified in the presence or absence of its cognate ligand E2.

Results: From a library of 570 human cDNA clones, we identified zinc finger protein 131 (ZNF131) as a repressor of ER alpha mediated transactivation. ZNF131 is a typical member of the BTB/POZ family of transcription factors, and shows both ubiquitous expression and a high degree of sequence conservation. The luciferase reporter gene assay revealed that ZNF131 inhibits ligand-dependent transactivation by ER alpha in a dose-dependent manner. Electrophoretic mobility shift assay clearly demonstrated that the interaction between ZNF131 and ERa interrupts or prevents ER alpha binding to the estrogen response element (ERE). In addition, ZNF131 was able to suppress the expression of pS2, an ER alpha target gene.

Conclusion: We suggest that the functional screening platform we constructed can be applied for high-throughput genomic screening candidate ER alpha-related genes. This in turn may provide new insights into the underlying molecular mechanisms of ER alpha regulation in mammalian cells.

语种英语
WOS记录号WOS:000260679600001
项目编号2006AA02A305
资助机构National High Technology Research and Development
引用统计
被引频次:9[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/58154
专题北京大学基础医学院_免疫学系
作者单位1.Beihua Univ, Jilin 132013, Peoples R China
2.Chinese Natl Human Genome Ctr, Beijing 100176, Peoples R China
3.Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Lab Med Immunol, Beijing 100191, Peoples R China
4.Peking Univ, Ctr Human Dis Genom, Beijing 100191, Peoples R China
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GB/T 7714
Han, Xiao,Guo, Jinhai,Deng, Weiwei,et al. High-throughput cell-based screening reveals a role for ZNF131 as a repressor of ERalpha signaling[J]. BMC GENOMICS,2008,9(0).
APA Han, Xiao.,Guo, Jinhai.,Deng, Weiwei.,Zhang, Chenying.,Du, Peige.,...&Ma, Dalong.(2008).High-throughput cell-based screening reveals a role for ZNF131 as a repressor of ERalpha signaling.BMC GENOMICS,9(0).
MLA Han, Xiao,et al."High-throughput cell-based screening reveals a role for ZNF131 as a repressor of ERalpha signaling".BMC GENOMICS 9.0(2008).
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